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Home :: Acute Tubular Necrosis

Acute Tubular Necrosis

Alternative names :- Necrosis - renal tubular; ATN; Necrosis - acute tubular

Also known as acute tubulointerstitial nephritis, acute tubular necrosis (ATN) accounts for about 75% of all cases of acute renal failure. Its the most common cause of acute renal failure in critically ill patients. ATN injures the tubular segment of the nephron, causing renal failure and uremic syndrome. Mortality ranges from 40% to 70%, depending on complications from underlying diseases. Nonoliguric forms of ATN have a better prognosis.


ATN results from ischemic or nephro­toxic injury, most commonly in debilitated patients, such as the critically ill and those who have undergone extensive surgery.

In ischemic injury, disruption of blood flow to the kidneys may result from circulatory collapse, severe hypotension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, or reactions to transfusions. Ischemic ATN can damage the epithelial and basement membranes and can cause lesions in the renal interstitium.

In nephrotoxic injury, damage may follow ingestion of certain chemical agents or result from a hypersensitive reaction of the kidneys. Because nephrotoxic ATN doesn't damage the basement membrane of the nephron, it's potentially reversible.

ATN may result from:

  • diseased tubular epithelium that allows leakage of glomerular filtrate across the membranes and reabsorption of filtrate into the blood
  • obstruction of urine flow by the collection of damaged cells, casts, red blood cells (RBCs), and other cellular debris within the tubular walls
  • ischemic injury to glomerular epithelial cells, resulting in cellular collapse and decreased glomerular capillary permeability
  • ischemic injury to vascular endothelium, eventually resulting in cellular swelling and obstruction.

Signs and symptoms

ATN is usually difficult to recognize in its early stages because effects of the critically ill patient's primary disease may mask the symptoms of ATN. The first recognizable effect may be decreased urine output. Generally, hyperkalemia and the characteristic uremic syndrome soon follow, with oliguria (or, rarely, anuria) and confusion, which may progress to uremic coma. Other possible complications include heart failure, uremic pericarditis, pulmonary edema, uremic lung, anemia, anorexia, intractable vomiting, and poor wound healing due to debilitation.

Fever and chills are ominous signs of infection, the leading cause of death in ATN.


ATN is hard to diagnose accurately until it has progressed to an advanced stage. The most significant laboratory clues are urinary sediment containing RBCs and casts and diluted urine with a low specific gravity (1.010), low osmolality « 400 mOsmlkg), and high sodium level (40 to 60 mEq/L).

Blood studies reveal elevated blood urea nitrogen and serum creatinine levels, anemia, defects in platelet adherence, metabolic acidosis, and hyperkalemia. An electrocardiogram may show arrhythmias (from electrolyte imbalances) and, with hyperkalemia, a widening QRS segment, disappearing P waves, and tall, peaked T waves


Vigorous supportive measures are required during the acute phase of ATN until normal kidney function resumes.

Initial treatment may include administration of diuretics and infusion of a large volume of fluids to flush tubules of cellular casts and debris and to replace fluid loss. However, this treatment carries a risk of fluid overload. Long­term fluid management requires daily replacement of projected and calculated losses (including insensible loss).

Other appropriate measures to control complications include transfusion of packed RBCs for anemia and administration of antibiotics for infection. Hyperkalemia may require emergency I. V. administration of 50% glucose, regular insulin, and sodium bicarbonate. Sodium polystyrene sulfonate with sorbitol may be given orally or by enema to reduce extracellular potassium levels. Peritoneal dialysis or hemodialysis may be needed if the patient is catabolic.

Special considerations
  • Maintain fluid balance. Watch for fluid overload, a common complication of therapy. Accurately record intake and output, including wound drainage, nasogastric output, and peritoneal dialysis and hemodialysis balances. Weigh the patient daily.
  • Monitor hemoglobin (Hb) level and hematocrit, and administer blood products as needed. Use fresh packed cells instead of whole blood to prevent fluid overload and heart failure.
  • Maintain electrolyte balance. Monitor laboratory results, and be alert for evidence of imbalances. Enforce dietary restriction of foods containing sodium and potassium, such as bananas, orange juice, and baked potatoes. Check for potassium content in prescribed medications (for example, penicillin G potassium and penicillin V potassium).
  • To maintain an anabolic state, provide adequate calories and essential amino acids, while restricting protein intake. Total parenteral nutrition may be indicated in the severely debilitated or catabolic patient.
  • Use aseptic technique, particularly when handling catheters, because the debilitated patient is vulnerable to infection. Watch for fever, chills, delayed wound healing, or flank pain if the patient has an indwelling urinary catheter in place.

Expectations (prognosis)

The duration of symptoms of ATN is variable. The decreased urine output phase may last from a few days to 6 weeks or more. This is occasionally followed by a period of high urine output, where the healed and newly refunctioning kidneys attempt to clear the body of fluid and wastes. One or two days after urine output rises, symptoms reduce and laboratory values begin to return to normal.

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